Comments were received from the following individuals and organizations during the public consultation on the draft WHO Guideline: Sugars intake for adults and children Government agencies Douglas Ackerman

Florida Department of Citrus, USA

Nawal Alhamad Alhamad

Food & Nutrition Administration, Ministry of Health, Kuwait

Donald Barker

Alberta Health Services, Canada

Lisette Brink

The Netherlands Nutrition Centre, Netherlands

Patricia Cecilia Cardoso

Administración Nacional de Medicamentos, Alimentos y Tecnología Médica - ANMAT, Argentina

Lara Comi

European Parliament, Italy

Yuk Ching Alex Fu

Department of Health, Hong Kong Special Administrative Region Government, China

Elisabetta Gardini

European Parliament, Italy

Andrea Ghiselli

Research Center on Food and Nutrition (CRA-NUT), Agricultural Research Council (CRA), Italy

Dr Cho-Il Kim

Korea Health Industry Development Institute, Republic of Korea

Dr Sebastián Laspiur

Ministerio de Salud de la Nación (Ministry of Health), Argentina

Dr Isra Levy

Ottawa Public Health, Canada

Fabienne Meier

Federal Food Safety and Veterinary office FSVO

National Food Institute

National Drugs, Foods and Medical Technology Administration, Argentina

Eduardo Augusto Fernandes Nilson

Ministry of Health, Brazil

Public Health England

Public Health England, United Kingdom

Leanne Rodine

Alberta Health Services, Canada

Dr Barbara Seed

Supreme Council of Health, Qatar

1

Rusidah BT Selamat

Nutrition Division, Ministry of Health, Malaysia

Dr Robert Strang

Nova Scotia Department of Health and Wellness, Canada

Eretii Teretia Timeon

Nutrition Center, Ministry of Health, Kiribati

Blanca Cecilia Hernández Torres, Yenny Consuelo Velosa Melgarejo

Ministerio de Salud y Protección Social, Colombia

Maria Vezzoni

Public Health Unit - Azienda Sanitaria Locale Milano 2, Italy

Suvi Virtanen

National Institute for Health and Welfare, Finland

Anna Zaborska

European Parliament, Slovakia

UN agencies Saskia De Pee

World Food Programme, Italy

Benoit Varenne

WHO Regional Office for Africa, Democratic Republic of the Congo

Nongovernmental and consumer organizations and associations Cary Adams The NCD Alliance, Switzerland David Arnold

British Dental Health Foundation, United Kingdom

Bridget Benelam

British Nutrition Foundation, United Kingdom

Professor ED Berman, MBE

Inter-Action Social Enterprise Trust, United Kingdom

Dr Alison Boyd

Sugar Nutrition UK, United Kingdom

Xaviera Cabada

El Poder del Consumidor AC, Mexico

Pauline Castres

BEUC (European Consumer Organisation), Belgium

Dr David Cavan

International Diabetes Federation (IDF), Belgium

Sylvia Cheater

Food Act!ve, United Kingdom

2

Sylvia Cheater

Heart of Mersey, United Kingdom

Helen Cherrett

American Dental Association, USA

Janet E Collins

Institute of Food Technologists, USA

Dr Noelle Cotter, Dr Helen Mcavoy, Mr Owen Metcalfe

Institute of Public Health in Ireland (IPH), Ireland

Helen Crawley

First Steps Nutrition Trust, United Kingdom

Jean-Luc Eisele

FDI World Dental Federation, Switzerland

Jan Frank PhD

The Society of Nutrition and Food Science, Germany

Lisa Gable

Healthy Weight Commitment Foundation, USA

German Nutrition Society

German Nutrition Society, Germany

Pietro Giordano

ADICONSUM, Italy

Suzanne S Harris

International Life Sciences Institute, USA

Claire Hewat

Dietitians Association of Australia, Australia

Michael F Jacobson

Center For Science in the Public Interest, USA

Bill Jeffery

Centre For Science in the Public Interest , Canada

Steven Jenkins

The British Dietetic Association, United Kingdom

Mariell Jessup MD

American Heart Association/American Stroke Association, USA

Therese Junker

Swiss Heart Foundation, Switzerland

Ms Etain Kett

Dental Health Foundation, Ireland

Prof Berthold Koletzko (On Behalf Of FISPGHAN)

Federation of International Societies on Paediatric Gastroenterology, Hepatology and Nutrition (FISPGHAN), Germany

3

Tim Lobstein

World Obesity Federation, Formerly The International Association For The Study of Obesity (IASO) and The International Obesity Taskforce (IOTF), United Kingdom

Susanne Logstrup

European Heart Network (EHN), Belgium

Professor Graham Macgregor

Action On Sugar, Wolfson Institute of Preventive, Medicine Barts and The London School of Medicine & Dentistry, Queen Mary University of London, United Kingdom

Annette Matzke

NGO-Alliance Nutrition, Physical Activity and Body Weight, Switzerland (Cardiovasc Suisse, Swissheart, Forum Obesity Schweiz, Swiss Ligue Contre Cancer, Swiss Society of Public Health, Swiss Society of Nutrition SSN, Alliance of Swiss Consumers’ Organisations), Switzerland

Aileen Mcgloin

Safefood, Ireland

Mariska Meurs

Wemos Foundation, Netherlands

Janis Morrissey

Irish Heart Foundation, Ireland

Modi Mwatsama

UK Health Forum and WCRF International, United Kingdom

Dr Robert Nuttall

Canadian Cancer Society, Canada

Sarah D Ohlhorst, MS RD

American Society for Nutrition, USA

Peter Pachner

Austrian Association for Public Health, Austria

Barbara Pfenniger

Fédération Romande des Consommateurs, Switzerland

Patti Rundall

Baby Milk Action, United Kingdom

Gerhard Konrad Seeberger

Italian Dental Association, AIO, Italy

Dorota Sienkiewicz

European Public Health Alliance (EPHA), Belgium

Terry Slevin

Cancer Council Western Australia, Australia

Amy Smullen

British Heart Foundation, United Kingdom

Elisabeth Sterken

International Baby Food Action Network, Canada

4

Maurice Swanson

Heart Foundation WA, Australia

Akikazu Takada

International Projects on Food and Health, Japan

Dr Georgios Tsakos

European Association of Dental Public Health, United Kingdom

Dr Janine Verheesen

Knowledge centre Sugar & Nutrition, Netherlands

Derek Yach

Executive Director; Vitality Institute (Part of Discovery Holdings, South Africa), USA

Private sector (including industry organizations and associations) Monica Elizondo Andrade Camara Costarricense de Industria Alimentaria, Colombia Dr Geoffrey Annison

Australian Food and Grocery Council, Australia

Charles W Baker

Sugar Association, Inc, USA

Sharon Bligh

The Consumer Goods Forum, France

Leon H Bruner, DVM, PhD

Grocery Manufacturers Association, USA

Massimo Camperi

Ferrero Asia LTD, Singapore

J Agustin Valencia Dongo Cardenas

ASBEGA (Asociación de la Industria de Bebidas Gaseosas del Peru), Peru

Arianna Carughi PhD

Sun-Maid Growers of California, USA

Igor Von Broesigke Castro

Brazilian Association of Soft Drink and Non Alcoholic Beverages, Brazil

Richard Conrad Cottrell

World Sugar Research Organisation, United Kingdom

Maria Agnese Dau

Federalimentare - Italian Food & Drink Industry Federation, Italy

Mauro Fontana

Soremartec Italia SRL (Ferrero Group), Italy

Jamie Fortescue

European Starch Industry Association, AAF, Belgium

Jim Goetz

Canadian Beverage Association, Canada

5

Christine Teuna Fennie Grit

Federatie Nederlandse Levensmiddelen Industrie (FNLI) Dutch Food and Groceries' Association, Netherlands

Barbara Groele

Krajowa Unia Producentów Soków (KUPS) - Polish Association of Juices Producers, Poland

Juan Fernando Gutierrez

Proyectos, Ecuador

Emilio Herrera

Asociacion Nacional de Productores de Refrescos y Aguas Carbonatadas, AC, Mexico

Ellen Hof

ENSA - European Natural Soyfoods Manufacturers Association, Belgium

Delon Human

International Food & Beverage Alliance, Switzerland

Carole May Inkster

New Zealand Food & Grocery Council, New Zealand

International Federation Of Fruit Juice Producers (IFU)

IFU, France

Edmundo Klotz

ABIA – Brazilian Association of Food Industries, Brazil

Dr Angela Kohl

German Federation for Food Law and Food Science (BLL), Germany

Katherine W Loatman

International Council of Beverages Associations, USA

Carolina Lorduy

Chamber of the Food Industry of the National Association of Colombia (ANDI), Colombia

Emilie Majster

European Committee of Sugar Manufacturers (CEFS), Belgium

Roberto Menta, MD PhD

Soremartec Italia SRL (Ferrero Group), Italy

Hugo Miguens

Camara Argentina de la Industria de Bebidas sin Alcohol (CADIBSA), Argentina

Sabine Nafziger

Chocolate, biscuits & confectionery of Europe (CAOBISCO), Belgium

Carolina Muro Niño

Spanish Food and Drink Industry Federation, Spain

Dominic Nolan

Australian Sugar Industry Alliance, Australia

Ing Gloria Cervera Perez

Camara Nacional del Maiz Industrializado (CANAMI), Mexico 6

Mario Piccialuti

AIDEPI, Italian Association of Confectionery and Pasta Industries, Italy

Andrea Poli

NFI- Nutrition Foundation of Italy, Italy

Andrew Resnick

Corn Refiners Association, USA

Francisco Roberto Herrarte Rivera

Gremial de Fabricantes de Alimentos (GREFAL), Guatemala

Dr Anne Roulin

Nestlé, Switzerland

Laurence Rycken

International Dairy Federation, Belgium

Sara Salvatore

Ferrero SPA, Italy

Ding Shaohui

China National Confectionery Association, China

Lurdes Soares

AIJN - European Fruit Juice Association, Belgium

Haley Stevens

Calorie Control Council, USA

Fuad Chiver Sucri

Asociación Nacional de Fabricantes de Chocolates, Dulces y Similares AC, Mexico

Jennifer Thompson

Australian Industry Group (Ai Group) - Confectionery Sector, Australia

Unionzucchero

Unionzucchero - Unione Nazionale Fra Gli Industriali Dello Zucchero, Italy

Maisie Vanriel

Food and Consumer Products of Canada, Canada

Dr Stefania Vezzosi

ANDID - Italian Association of Dietitians, Italy

Flora Wang

Canadian Sugar Institute, Canada

Diane Welland

Juice Products Association, USA

John S White, PhD

White Technical Research, USA

Martin Wickham

Leatherhead Food Research, United Kingdom

7

Sarah Wingensiefen

Wirtschaftliche Vereinigung Zucker EV, Germany

Geoffrey Woolford, PhD

Ocean Spray Cranberries, Inc, USA

Academic Dennis M Bier, MD

Baylor College of Medicine, USA

Salmeh Bahmanpour

Shiraz University of Medical Sciences, Iran (Islamic Republic of)

Eduardo Bernabe

King's College London, Dental Institute, United Kingdom

Jennifer Bernal

Universidad Simón Bolívar / University of South Carolina, USA

Pierre Bougneres

Paris Sud University, INSERM, France

Giorgio Calabrese

University Federico II - Naples, Italy

Carmen Gomez Candela

Nutrition Department, Hospital University La Paz; University Automa of Madrid, Spain

Professor Dr W Crielaard, Professor Dr C Van Loveren

ACTA, Netherlands

Edith Feskens

Wageningen University, Division of Human Nutrition, Netherlands

Jan MC Geuns

KU Leuven, Belgium

Maria Raquel de Assunção Gonçalves e Silva

University Fernando Pessoa, Oporto, Portugal

Luis Eduardo García Gonzalez

Metabolic Syndrome, Obesity and Malnutrition Clinics, Juarez Autonomous University of Tabasco, Mexico

Mairéad Heffron

Royal College of Physicians of Ireland (RCPI), Ireland

Karen Hofman

University of Witwatersrand School of Public Health, South Africa

Cristin E Kearns, DDS MBA

University of California San Francisco, USA

Professor Amanda Lee

Queensland University of Technology, Australia

8

Livio Luzi

University of Milan, Italy

Dr Sean Mark

School of Population and Public Health, University of British Columbia, Canada

Sara Esther Valdés Martinez

Universidad Nacional Autónoma de México; Facultad de Estudios Superiores Cuautitlán; Laboratorio de Tecnología de Calidad en Alimentos, Mexico

Anne-Thea Mcgill

University of Auckland, New Zealand

Lindsey Morse

Imperial College, United Kingdom

Marco Peres, Jane Harford, Katrina Plastow, Jenny Miller

Australian Research Centre for Population Oral Health, School of Dentistry, The University of Adelaide, Australia

Len Piche, PhD RD

Nutrition, Brescia University College, Canada

Dr Phusit Prakonsai

International Health Policy Program (IHPP), Thailand

Andrew J Rugg-Gunn

Newcastle University, United Kingdom

Dr Arun K Simon

Manipal College of Dental Sciences, Manipal University, India

Yi-Xiang Su

School of Public Health, Sun Yat-Sen University, China

Professor Eugenio Del Toma

Campus Biomedico, Rome University, Italy

Bernhard Watzl

Max Rubner-Institute, Federal Research Institute of Nutrition and Food, Germany

Mark Weiss

UK Faculty of Public Health, United Kingdom

Shigeru Yamamoto, PhD RD

Ajian Nutrition and Food Culture Research Center, Jumonji University, Japan

Other individuals Faye Cheeseman

Private citizen, United Kingdom

Jocelyn Guillot-Narvaez

Bariatric Friendly, USA

Susan Lesch

Private citizen

9

Bernard Morre

Private citizen, France

Benjamin Seeds

Private citizen, Switzerland

Sergio Pumarola Segura

Open Innovation Consultant, Spain

The Reverand Nathan D. Pipho

Evangelical Lutheran Church In America, USA

Zoe Eaton

I Quit Sugar, Australia

Mary-Kate Hoogland

Sustainable Health, Australia

Dr DS Prasad, MD PhD

Sudhir Heart Centre, India

10

Summaries of comments received

Assessment and response

Weight gain, as a risk factor for diabetes and other major NCDs, should be clearly distinguished from the effects of sugar on dental health throughout the guideline. Furthermore, an excessive intake of free sugars can lead, not only to overweight, but to an excess of visceral fat which is associated with insulin resistance, and can lead to type 2 diabetes in a person with normal body weight. Therefore, statements which restrict the link between high sugar intake and NCDs to its effect on body weight, do not address the whole dimension of the problem. Evidence also exists on the direct effects of free sugars intake (in the form of sugar-sweetened beverages) and type 2 diabetes as well as cardiovascular diseases. Therefore, discussions of sugars intake and diabetes and cardiovascular diseases and the risk of developing those NCDs should be included in the guideline. Speaking only about obesity and caries looks less important for health when you speak with the public as the recommendations seem to have purely focused on aesthetic goals (i.e. obesity and dental caries) whereas WHO’s goals should be to provide recommendations to reduce the risk of NCDs in adults and children.

As stated in the guideline, when determining the scope of the guideline, the WHO Nutrition Guidance Expert Advisory Group (NUGAG) Subgroup on Diet and Health decided unhealthy weight gain and dental caries as the priority health outcomes to be focused on when undertaking the systematic reviews. This was in recognition of the rapidly growing epidemic of overweight and obesity around the globe and its role as a risk factor for several NCDs. In addition, dental caries is the most common NCD, and the cost of its treatment places a heavy burden on health-care budgets in many countries. But a need for systematic reviews and meta-analyses related to free sugars intake and blood lipid levels, blood pressure and diabetesrelated outcomes (i.e. glucose, insulin, metabolic syndrome, prediabetes and insulin resistance) is suggested in the “Implications for future research” section of the guideline. It should be noted that while the finalization of the guideline was underway, a new systematic review was published in May 2014 by Te Morenga et al. which provided evidence that free sugars may influence cardiometabolic risk factors independently of changes in body weight, suggesting that a reduction in free sugars intake may also be beneficial for reducing risk of cardiovascular diseases. As such, this new systematic review also supports the recommendation to reduce intake of free sugars for health benefits.

Considering obesity and dental caries together is conceptually wrong. Obesity is a complex systemic disorder associated with hypertension, diabetes, cardiovascular diseases and dyslipidemia in the context of metabolic syndrome, while dental caries is a local effect of free glucose. Since the etiopathogenesis of obesity and dental caries are different, (and since the evidence for thresholds is based only on studies of dental caries), the recommendations to prevent those diseases should also be different.

How and why unhealthy weight gain and dental caries have been identified as priority healthy outcomes for developing this guideline are described in the “Scope and purpose” section of the guideline.

In the WHO Global Status Report on Noncommunicable Diseases 2010, the following four NCDs are listed: cardiovascular diseases, cancers, diabetes and chronic respiratory diseases. The NCD Global Action Plan 2013-2020 also focuses on these four NCDs. In the present

It is noted in the NCD Global Status Report that the primary focus of the report was on the four groups of diseases (i.e. cardiovascular diseases, cancers, diabetes and chronic lung diseases) which are responsible for the majority of deaths caused by NCDs and are largely caused by four shared 11

guideline, dental caries is also listed as an NCD. We prefer a more consistent communication and information and we would therefore appreciate putting the main focus on the four main NCDs (i.e. cardiovascular diseases, cancers, diabetes and chronic respiratory diseases).

behavioural risk factors. While the broader scope of noncommunicable conditions are not specifically addressed by the content and focus of the report, many of the approaches and opportunities for tackling NCDs described are also directly relevant to these conditions. It was not possible to state all NCD issues in the guideline; therefore, in the guideline, the reference was made to both the 2010 and 2014 NCD Global Status Reports where detailed information on NCDs can be found.

We suggest to include a reference not only to mortality as such, but in particular to premature mortality, a phenomenon illustrating a worrisome trend in relation to the NCDs from modifiable, avoidable – and to a great degree – unequally and unfairly distributed risk factors such as diets of poor nutritional quality. This is also particularly valid in the case of overweight and obesity which are a comorbidity of type 2 diabetes, certain cancers and cardiovascular diseases.

The “Background” section of the guideline is updated with the data provided in the 2014 NCD Global Status Report which also provides data on premature death.

The Codex Alimentarius, as the body that sets international food standards, guidelines and codes of practice for food and the food system, should be informed of the recommendations and ways should be identified as to how the Codex can or should use these recommendations.

WHO regularly informs relevant Codex Committees, such as the Codex Committees on Food Labelling (CCFL), and Nutrition and Food for Special Dietary Uses (CCNFSDU) of new and updated WHO nutrition guidelines and recommendations in order to encourage and ensure the use and incorporation of WHO guidelines in their on-going work in developing Codex standards and guidelines.

There is a need to stress the differences between this guideline and TR 916. TRS 916 addressed all major dietary and other issues to major NCDs and recommended guidelines on whole diet and active living. So the context is very different from this guideline which takes one nutrient and develops guidance for it without taking into consideration the needed changes in total calorie intake, i.e. shifts in intakes of fats and oils (that could result as people substitute one set of nutrients for another).

As noted in the guideline, this guideline is developed as part of the ongoing efforts of WHO to update existing dietary goals for the prevention of NCDs which was last updated in 2002 by the WHO/FAO Expert Consultation (TRS916 is the report of this expert consultation). Since the 2002 WHO/FAO Expert Consultation, the WHO guideline development process has changed as described in the WHO handbook for guideline development (2014), in order to implement procedures to ensure that WHO guidelines are developed in ways consistent with best practices, emphasizing the appropriate use of evidence. This change of the guideline development process led to the development of guidelines for each nutrient, given the available resources. The guideline development process that was implemented to develop this guideline is described in detail in the guideline. The guideline also highlights the need to use it in 12

conjunction with other nutrient guidelines and dietary goals, in particular those related to fats and fatty acids in order to guide effective public health nutrition policies and programmes to promote a healthy diet. During the public consultation, it should be allowed for people to provide different and other possible studies and data that should also be included as additional evidence in order to improve the transparency of WHO’s guideline development process.

As described in the guideline, WHO follows the guideline development process which is guided by the WHO handbook for guideline development (2014).

The BMI chart used in a Pacific country states that normal BMI is 22-27, overweight is BMI 27-32, and obese is BMI > 32. Could this be highlighted as well in this guideline or should we (Pacific islanders) use the WHO's recommendation?

Discussing the BMI cut-off points for different population groups is beyond the scope of this guideline. The guideline included WHO BMI cut-off points to define overweight and obesity for the purpose of international comparison.

The 2007 FAO/WHO Scientific Update on Carbohydrates in Human Nutrition stated that there is no convincing scientific justification for differentiating between “free”, “added” and “other” sugars. All sugars, whether added or naturally occurring, provide 4 kcal/gram, and have the same effect on health. There is no scientific evidence that the human body makes any physiological distinction between sugars that are added to foods and those that are naturally occurring. We further note that analytical techniques are unable to distinguish between sugars that are added to foods and naturally occurring sugars, as they are chemically identical. Therefore, the WHO Draft Guideline’s focus on “free sugars” is unwarranted and has the potential to mislead consumers, and risks reinforcing misperceptions that added sugars are somehow more caloric or otherwise different from sugars inherent in many foods or beverages. It should also be noted that the Cummings & Stephen paper which was produced as part of the 2007 FAO/WHO Scientific Update on Carbohydrates in Human Nutrition states that “total sugars” is the term more widely recognised and is most useful.

In the paper prepared by Cummings & Stephen for the 2007 FAO/WHO Scientific Update on Carbohydrates in Human Nutrition, they stated that the term “total sugars” is probably the most useful way to describe and measure sugars “for labelling purposes”. The key point they highlighted is related to measurement and labelling. It may be difficult to distinguish sugars present in the different compartments of a food or meal (i.e. intracellular or extracellular, from milk or fruit or vegetables). Therefore, Cummings & Stephen noted that the first step in any analysis and for labelling should be total sugars. But with regard to the physiology, the rate of digestion and absorption are determined by the physical properties of the food/meal in which the sugars are found. Therefore, consuming sugars as whole fruit (i.e. intrinsic sugars) would be different from consuming sugars as fruit juices (i.e. free sugars) in terms of the glycaemic, insulinaemic and satiety responses. Thus analytically these sugars are not different, but physiologically they are. As noted in various comments received, improved communication to the consumers and development of effective communication strategies and materials could facilitate the understanding of the recommendations which will lead to effective implementation of the guideline.

The statement that “free sugars contribute to the overall energy density of diets” is misleading since all macronutrients add energy density to the diet. All sugars contribute 4 kcal/gram, whereas fat

As stated in the guideline, the objective of the guideline is to provide recommendations on the intake of free sugars to reduce the risk of NCDs in adults and children, with a particular focus on the 13

contributes 9kcal/gm. If the main concern is the energy density of the diet, the guideline should be made on the amount of all macronutrients in the diet and thus the amount of calories that should be eaten, not just on the amount of free sugars in the diet. A calorie is a calorie and excess energy intake in any form will contribute to weight gain.

prevention and control of unhealthy weight gain and dental caries. Both the 1989 WHO Study Group and 2002 WHO/FAO Expert Consultation reviewed global and regional food consumption patterns and trends as well as dietary changes in some countries as part of their work and stated, (in the 2002 WHO/FAO Expert Consultation in particular), that free sugars contribute to the overall energy density of diets and when the energy density of the diet is increased, total energy intake is increased, citing a number of studies on the subject. As clearly indicated in the “Translation and implementation” section of the sugars guideline, the guideline should be used in conjunction with other nutrient guidelines and dietary goals, in particular those related to fats and fatty acids (including saturated fatty acids and trans-fatty acids), to guide effective public health nutrition policies and programmes to promote a healthy diet. WHO also provides guidance on healthy diet (i.e. Fact Sheet No 394, September 2014) which translates various nutrient guidelines that WHO develops and updates as part of its normative work.

The claim that high levels of free sugars intake is associated with poor dietary quality are not supported by evidence. The relationship between sugars intake and the nutrient quality of diets was not reviewed in the current exercise and was not reviewed in the previous two WHO expert consultations that are cited as reference for this claim.

Both the 1989 WHO Study Group and 2002 WHO/FAO Expert Consultation reviewed global and regional food consumption patterns and trends as well as dietary changes in some countries as part of their work and stated,(in the 2002 WHO/FAO Expert Consultation in particular), that free sugars contribute to the overall energy density of diets and when the energy density of the diet is increased, total energy intake is increased, citing a number of studies on the subject.

The evidence supporting the recommendation is based on studies in which it was determined that changes in total energy intake were responsible for changes in body weight and not from consumption of free sugars per se: free sugars do not affect body weight when isocalorically substituted for other nutrients. This is not prominently noted in the guideline.

A statement, "The excess body weight associated with free sugars intake results from excess energy intake" is included in the “Remarks” section of the guideline to highlight the importance of energy balance.

Increased free sugars intake may result in weight gain under ad libitum conditions; however, this is also true of dietary fat and is primarily an effect of food energy density. Conversely, similar effects in terms of preventing weight gain can be achieved by reducing either fat or free sugars intake with a goal of limiting energy intake.

As clearly indicated in the “Translation and implementation” section, the guideline should be used in conjunction with other nutrient guidelines and dietary goals, in particular those related to fats and fatty acids (including saturated fatty acids and trans-fatty acids), to guide effective public health nutrition policies and programmes to promote a 14

healthy diet. WHO also provides guidance on healthy diet (i.e. Fact Sheet No 394, September 2014) which translates various nutrient guidelines that WHO develops and updates as part of its normative work. WHO Consultation on Obesity (TRS 894) commented “Dietary fat has a higher energy density than other macronutrients. This is thought to be largely responsible for the overeating effect, or passive overconsumption as it is often called, experienced by many subjects exposed to high-fat foods”. Thus a reduction in sugar intake might lead to an increase, rather than a decrease, in the prevalence of obesity, if free sugars are replaced by dietary fats. A FAO/WHO Expert Consultation has commented under Principles of carbohydrate food choices “to acknowledge that there may be unintended consequences involved in carbohydrate food intake change, and also to ensure that risks involved in dietary changes from traditional diets is considered”. National policies to restrict consumption of sugars might therefore not only be expensive and ineffective, but could damage the public’s health by inadvertently leading to higher consumption of fats.

In order to avoid such unintended consequences, it is indicated clearly in the “Translation and implementation” section that this guideline should be used in conjunction with other nutrient guidelines and dietary goals, in particular those related to fats and fatty acids (including saturated fatty acids and trans-fatty acids), to guide effective public health nutrition policies and programmes to promote a healthy diet. This is a nutrient guideline which needs to be translated into culturally and contextually specific food-based dietary guidelines that take into account locally available food and dietary customs at the country level. Information on how the recommendations of the guideline can be translated into action is provided in the “Translation and implementation” section of the guideline.

The observed effects on body weight are small, such that the findings cannot be extrapolated to population-based advice.

The recommendations in the guideline target individuals, not populations.

When assessing the effects of consuming a particular nutrient on body weight, an individual’s total energy intake, their nutritional, socioeconomic and cultural status, access to foods and other factors must also be considered. The etiology of obesity is multifactorial and approaches to prevention should be addressed from the perspective of overall healthy lifestyle.

This is a nutrient guideline which needs to be translated into culturally and contextually specific food-based dietary guidelines that take into account locally available food and dietary customs at country level. Information on how the recommendations of the guideline can be translated into action is provided in the “Translation and implementation” section of the guideline. The guideline also highlights the need to use it in conjunction with other nutrient guidelines and dietary goals, in particular those related to fats and fatty acids in order to guide effective public health nutrition policies and programmes to promote a healthy diet. WHO also provides guidance on healthy diet (i.e. Fact Sheet No 394, September 2014) which translates various nutrient guidelines that WHO develops and updates as part of its normative work. Furthermore, comprehensive strategies to prevent and control NCDs (including obesity) are provided in the NCD 15

Global Action Plan 2013 - 2020 which was endorsed by the World Health Assembly in 2013. Weight gain is caused by energy imbalance (consuming more energy than expending through physical activity). The importance of physical activity was not stressed.

The importance of physical activity is addressed in various other WHO documents including Global recommendations on physical activity for health (2010). However, it should be noted that the guideline recognizes the importance of energy balance and therefore, a statement , "The excess body weight associated with free sugars intake results from excess energy intake" is included in the “Remarks” section of the guideline.

The role of portion size in weight gain is not considered. The guideline should promote healthy diet and lifestyles including the control of portion size to reduce the overall calorie intake.

In the "Translation and implementation" section of the guideline, some examples of how the recommendations of this guideline can be used by policy-makers, programme managers and other stakeholders are included. It is also stated that providing comprehensive overall dietary guidance, including other issues such as portion size, is beyond the scope of this guideline, because such guidance should be based on overall dietary goals that consider all required nutrients. WHO provides guidance on healthy diet (i.e. Fact Sheet No 394, September 2014) which translates various nutrient guidelines that WHO develops and updates as part of its normative work.

The studies included in the analysis of body weight include those with sugars and foods containing sugars as exposure/intervention. Foods containing sugars also contain other nutrients contributing to total energy intake. The review fails to indicate if this was accounted for.

The evidence for the effect of sugars on body weight is largely derived from randomized controlled trials of studies involving free living subjects. The intention in these randomized trials was to compare the effects of altering the proportion of total energy provided by free sugars without altering overall macronutrient distribution. When energy intakes were strictly controlled there was no effect of sugars on body weight. When not strictly controlled those consuming higher sugars diets did not adequately compensate for the additional energy provided by increased sugars by reducing intake of other energy sources. Similarly when subjects reduced their sugars intake they did not adequately compensate for the reduction by increasing intake of other energy sources.

Many of the body weight studies involved an explicitly counselled or mandatory consumption of an added energy load as sugars, and compared this to a lower-energy or energy-free load. Thus, it is not clear if these are really a test of sugars specifically or supplemental energy in general.

The evidence for the effect of sugars on body weight is largely derived from randomized controlled trials of studies involving free living subjects. The intention in these randomized trials was to compare the effects of altering the proportion of total energy provided by free sugars 16

without altering overall macronutrient distribution. When energy intakes were strictly controlled there was no effect of sugars on body weight. When not strictly controlled those consuming higher sugars diets did not adequately compensate for the additional energy provided by increased sugars by reducing intake of other energy sources. Similarly when subjects reduced their sugars intake they did not adequately compensate for the reduction by increasing intake of other energy sources. In the evidence summary, clarification is needed as to how the effects of total energy intake were distinguished from the effects of free sugars intake in the body weight studies included in the systematic review.

Clarification can be found in the systematic review by Te Morenga et al. (2013). The evidence for the effect of sugars on body weight is largely derived from randomized controlled trials of studies involving free living subjects. The intention in these randomized trials was to compare the effects of altering the proportion of total energy provided by free sugars without altering overall macronutrient distribution. When energy intakes were strictly controlled there was no effect of sugars on body weight. When not strictly controlled those consuming higher sugars diets did not adequately compensate for the additional energy provided by increased sugars by reducing intake of other energy sources. Similarly when subjects reduced their sugars intake they did not adequately compensate for the reduction by increasing intake of other energy sources.

Most of the studies on body weight in children relate to liquid calories from sugar; thus there is no evidence of an association with free sugars from solid food and body weight in children.

There was no effect of reducing sugars (from beverages and foods) on body weight in the randomized controlled trials in children. Most of the 21 cohort studies in children included sugarsweetened beverages exclusively as the exposure but some of those with solid food exposures (e.g. snacks, candies, chocolates) demonstrated a positive association with body weight. The cohort studies that were subjected to GRADE analysis and subsequently used in the formulation of the recommendations all reported sugar-sweetened beverage exposures.

Some of the body weight studies were not representative of normal human behaviour (e.g. participants in some studies consumed very high or very low quantities of free sugars, in one case 438 grams per day) and thus have limited applicability in free-living populations.

Inclusion and exclusion criteria used in selecting studies were guided by the PICO questions which are described in detail in Annex 6 of the guideline, and in the systematic review by Te Morenga et al. (2013). Free sugars intake also varies widely in many populations. Exclusion of the study involving very high sugars intakes (i.e. 438 grams per day) did not influence the outcome. 17

The body weight analysis is based largely on shortterm intervention studies which have limited applicability in real world settings.

Inclusion and exclusion criteria used in selecting studies were guided by the PICO questions which are described in detail in Annex 6 of the guideline, and in the systematic review by Te Morenga et al. (2013). The need for longer term controlled trials of the effect of increasing or decreasing free sugars intake on body weight is noted in the “Implications for future research” section of the guideline.

Although an association between sugars intake and weight gain was observed in the analysis of body weight studies, it is unclear if the duration of many of the studies was sufficient to detect more significant changes in body weight.

Inclusion and exclusion criteria used in selecting studies were guided by the PICO questions which are described in detail in Annex 6 of the guideline, and in the systematic review by Te Morenga et al. (2013), which includes duration of the studies. These were discussed and agreed upon by the WHO Nutrition Guidance Expert Advisory Group (NUGAG) Subgroup on Diet and Health in order to determine the scope of the review. The need for longer term controlled trials of the effect of increasing or decreasing free sugars intake on body weight is recognized, and therefore noted in the “Implications for future research” section of the guideline.

A dose-response relationship between sugar intake and body weight was not observed which contradicts the statement that increasing or decreasing sugars intake is associated with parallel changes in body weight, regardless of the level of intake. No evidence for this statement has been provided.

A dose-response was not described in the systematic review, however, there was a consistent positive effect of higher sugars intakes on body weight at all levels of intake.

The evidence presented for body weight does not provide the rationale for the recommendations to reduce intake of free sugars to 10% and 5% of total energy intake.

As noted in the “Remarks” section of the guideline, thresholds were determined based on the evidence from analysis of the impact of free sugars intake on dental caries which was identified by the WHO Nutrition Guidance Expert Advisory Group (NUGAG) Subgroup on Diet and Health as a priority health outcome for developing recommendations for free sugars.

The evidence linking free sugars intake and body weight relies heavily on studies of sugarsweetened beverage consumption. Placing more emphasis on the contribution of sugar-sweetened beverages to intake of free sugars would provide a practical message to be incorporated into foodbased dietary guidelines.

The focus of the guideline is related to the intake of free sugars, not sugar-sweetened beverages, although sugar-sweetened beverages are included as one of the exposures when undertaking the systematic reviews, given their contribution to free sugars intake among various population groups. Additionally, this guideline is a nutrient guideline which then needs to be translated into culturally and contextually specific food-based dietary guidelines that take into account locally available 18

food and dietary customs at country level. Information on how the recommendations can be implemented and translated into action is also noted in the “Translation and implementation” section of the guideline which includes examples of measures that are already being implemented by countries, including food and nutrition labelling, regulation of marketing of foods and non-alcoholic beverages that are high in free sugars, and fiscal policies targeting foods and beverages that are high in free sugars. Sugar-sweetened beverages are the main source of added sugar in the daily diet of many children. The possible association between high intake of sugar-sweetened beverages and childhood obesity deserves more attention.

The focus of the guideline is related to the intake of free sugars, not sugar-sweetened beverages, although sugar-sweetened beverages are included as one of the exposures when undertaking the systematic reviews, given their contribution to free sugars intake among various population groups.

The recommendations should focus on sugarsweetened beverages as there are more supportive studies for this than for the broader category of free sugars.

Consumption of sugar-sweetened beverages was identified as one of the exposures, but not the only exposure, when developing the PICO questions (Annex 6) which guided the scope of the systematic reviews. As such, the evidence reviewed was not limited to sugar-sweetened beverages only. It is, therefore, not possible to make specific recommendation on sugar-sweetened beverages in this guideline.

Results from studies released since the publication of the systematic review (Ebbeling et al. [2012]; de Ruyter et. al. [2012]; Qi et al. [2012]), support the association between sugar-sweetened beverages and weight gain.

Comment noted.

Results from Ebbeling et al. (2012) and de Ruyter et. al. (2012) do not support an association between sugar-sweetened beverages and weight gain.

Overall the authors’ conclusion in both reviews cited in the comment was that intake of sugarsweetened beverages is associated with body weight. The detailed comments received during the public consultation indicating that the studies that do not show an association between sugarsweetened beverages select only certain aspects of the studies that support the assertion that there is no association (e.g. no effect was observed at the pre-specified 2 year time point in Ebbeling et al. [2012], but a significant effect was observed at 1 year; potential bias and a small but significant difference in BMI increase in de Ruyter et al. [2012]).

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The conclusions drawn regarding free sugars intake and body weight were based on the results of the meta-analysis by Te Morenga et al. (2013) which had limitations including risk of bias in some studies, publication bias and heterogeneity across studies. There was no convincing evidence from RCTs in adults that there was an effect of limiting dietary sugars on measures of body fatness when analysis was limited to studies that did not have a high risk of bias. In the adult cohort studies, only six of the 23 associations were statistically significant and these came primarily from one or two studies. No effect was observed in RCTs in children. In cohort studies, six out of several associations were significant and four reported a negative association. There are questions regarding the way some studies have been computed in the meta-analysis, which may have affected the magnitude of effect. The limitations of the review create uncertainty about the results and conclusions.

Study limitations are noted in the systematic review and addressed in the GRADE evidence profiles included in the guideline (Annex 1), which include a discussion of the effects of potential bias and heterogeneity on the strength of the recommendation, and are included in the guideline. No specific evidence provided regarding the comment questioning the way in which some studies have been computed in the meta-analysis. Similar comments addressing methodological questions about the systematic review that were published in peer-reviewed journals (i.e. BMJ) have already been answered in published replies from the authors.

The evidence does not support a causal association between sugar intake and weight gain, overweight or obesity.

The systematic review conducted by Te Morenga et al. (2013) suggests an association between sugars intake and body weight.

Fructose has a uniquely obesogenic effect, as it can't be metabolized by most body cells. Instead, it is metabolized by the liver, leading to fatty liver disease, insulin resistance and high blood pressure (via uric acid production, blocking endothelial nitric oxide), and the production of atherogenic LDL cholesterol, causing heart disease.

The focus of the guideline is related to the intake of free sugars which include monosaccharides (of which fructose is part) added to foods and beverages. Individual monosaccharides were not considered separately as exposures and it is not the intention of this guideline to provide specific recommendations on fructose per se.

Fructose is not uniquely obesogenic. Fructose is metabolised differently from glucose although evidence suggests that fructose is no more obesogenic than glucose (or other carbohydrates), nor does it appear to differ in its effect on insulin or markers of fatty liver disease. Fructose may have important advantages over glucose for body weight, glycaemic control and blood pressure.

The focus of the guideline is related to the intake of free sugars which include monosaccharides (of which fructose is part) added to foods and beverages. Individual monosaccharides were not considered separately as exposures and it is not the intention of this guideline to provide specific recommendations on fructose per se.

To inform the future application of the recommendations, it would have been useful to draw out from the review more detail about the amount and/or type of sugars consumption (increases or decreases in intake) that has a measureable effect on body weight.

The focus of this guideline is free sugars and details of the various studies that assessed different sugars exposures are provided in the systematic review on body weight by Te Morenga et al. (2013).

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The Te Morenga et al. (2013) review misrepresents the purpose of a number of studies and selects only part of their results.

There is no specific evidence of this noted in the comment. Comments addressing any methodological questions about the systematic review that were published in peer-reviewed journals (i.e. BMJ) have already been answered in published replies from the authors.

No randomized controlled trials in children were included in the analysis of free sugars intake and body weight.

Randomized controlled trials in children were included in the systematic review and metaanalysis by Te Morenga et al. (2013) which provided background evidence for developing the guideline.

Suggestions that free sugars, particularly in beverage form, are particularly obesogenic possibly as a result of a reduced ability to compensate for overall dietary energy intake is challenged by evidence suggesting that most of the energy consumed as sugar-sweetened beverages can be compensated for, resulting in little net gain in overall dietary energy.

While some studies suggest that most of the energy consumed as sugar- sweetened beverages can be compensated for, a substantial body of evidence suggests a reduced ability to compensate.

For interpretation, it is important to know over how long a time period the body weight studies contributing to the body weight analysis took place, how much the extra, or reduced, sugars intake contributed to additional, or reduced, energy intake, and whether or not there were other concurrent changes in dietary intake.

Details of the studies can be found in the systematic review by Te Morenga et al. (2013) which also provides references for all individual studies included in the systematic review.

The evidence seems to suggest that as long as energy intake is in balance with energy needs, the level of sugars does not matter, until it leads to inadequate intake of protein, fat and other essential nutrients. If a level at which this occurs is known, it would be good to state that.

The effect of altering sugars intakes by replacement with macronutrients other than carbohydrate was not assessed. The systematic review shows that subjects appear to increase energy intake when starchy carbohydrates are replaced with free sugars, or free sugars intakes increase. This appears due to inadequate compensatory reduction in other carbohydrate sources. However, the trials were ad libitum in nature and carried out in free living individuals, so it is possible that the interventions resulted in some differences in intakes of other macronutrients. Additionally, the logic used in this comment only considers the effects on body weight and ignores the effects of sugars intake on dental caries and, as suggested by recent publications, possible effects on cardiovascular disease risk.

The summary of the evidence on body weight does not appear to take into account the

As noted in the comments submitted, there are many examples of regional and national institutions 21

conclusions reached by other expert committees (e.g. EFSA [2010], IOM [2005], WHO/FAO [1997], UK Department of Health [1989], the Dietary Guidelines Advisory Committee convened by the US Department of Agriculture and the Department of Health and Human Services [2010], the guideline of the German Nutrition Society [2012]) regarding sugars intake and body weight.

or other bodies which have published guidelines and reports related to sugars intake and body weight. Therefore, it is not possible to select and consider the work of only a few such institutions in WHO guidelines. In terms of formulating recommendations, WHO conducts an independent review of the evidence following the WHO guideline development process as outlined in the WHO handbook for guideline development (2014), which includes rating the quality of evidence using GRADE methodology. Additionally, it should be noted that three of the positions to which this comment refers are taken from conclusions based on dated evidence (i.e. IOM [2005], FAO/WHO [1997], UK Department of Health [1989]). The current perspectives of other organizations providing dietary advice are in line with the WHO recommendations, including the American Heart Association, the European Heart Network and the UK Scientific Advisory Committee on Nutrition (draft report) which was issued for public consultation in May 2014 and is currently being finalized.

The guideline of the German Nutrition Society does not allow the conclusion that sugar is causally linked to the prevention of obesity, because no association of isocaloric exchange of sugar against other carbohydrates and weight change could be established.

There are many examples of regional and national institutions or other bodies which have published guidelines and reports related to sugars intake and body weight. However, for developing and updating dietary guidelines or recommendations, WHO conducts an independent review of the evidence following the WHO guideline development process as outlined in the WHO handbook for guideline development (2014), which includes rating the quality of evidence using GRADE methodology.

The Dutch Health Council concludes in the Guidelines for a healthy diet 2006, that there is insufficient evidence to make quantitative recommendations on free sugars intake with respect to the prevention of noncommunicable diseases.

There are many examples of regional and national institutions or other bodies which have published guidelines and reports related to sugars intake and NCDs. However, for developing and updating dietary guidelines or recommendations, WHO conducts an independent review of the evidence following the WHO guideline development process as outline in the WHO handbook for guideline development (2014), which includes rating the quality of evidence using GRADE methodology. After the review, the available evidence was considered sufficient to support recommendations on thresholds for free sugars intake as described in the guideline.

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Other bodies (EFSA, IOM) have not set thresholds for sugar intake on the basis of reducing risk of dental caries as the available evidence was considered insufficient to do so.

There are many examples of regional and national institutions or other bodies which have published guidelines and reports related to sugars and dental caries. However, for developing and updating dietary guidelines or recommendations, WHO conducts an independent review of the evidence following the WHO guideline development process as outline in the WHO handbook for guideline development (2014), which includes rating the quality of evidence using GRADE methodology. After the review, the available evidence was considered sufficient to support recommendations on thresholds for free sugars intake as described in the guideline.

There is no convincing evidence that sugar is addictive or encourages excessive or uncontrollable consumption.

Nowhere in the guideline is it suggested that sugars are addictive or responsible for uncontrollable consumption.

Since there is an association between reductions of free sugars intake and a reduction of body weight (principally based on a reduction of sugarsweetened beverages), an increase in water intake throughout the life-course should be recommended.

Comment noted.

Energy-dense diets, characterised by consumption of ultra-processed foods and beverages that are high in fat, sugar and salt, and low in nutrients and fibre, are the direct cause of the obesity pandemic.

Comment noted.

Excess weight gain, as one of the key outcomes of concern in relation to free sugars intake, is applicable to additional NCDs, including cancer. Being overweight or obese increases the risk of breast, colorectal, esophagus, kidney, pancreas and uterine cancer, and may increase the risk of ovarian and gallbladder cancer.

Comment noted.

In the US, where trends in intake and BMI data have been recently published, consumption of sugar-sweetened beverages have been declining while rates of obesity over the past decade have not changed.

The evidence and guidance presented in the guideline do not claim that sugars are the only macronutrient implicated in unhealthy weight gain. As noted in the guideline, this guideline on sugars intake should be used in conjunction with other nutrient guidelines and dietary goals, in particular those related to fats and fatty acids (including saturated fatty acids and trans-fatty acids), to guide effective public health nutrition policies and programmes to promote a healthy diet.

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The latest National Diet and Nutrition Survey data shows that sugar intake is reducing in nearly all groups of the UK population and yet obesity is increasing, therefore other factors (e.g. energy expenditure) must be involved.

The guideline notes the importance of energy balance in the “Remarks” section. In addition, it is stated that this guideline should be used in conjunction with other nutrient guidelines and dietary goals, in particular those related to fats and fatty acids (including saturated fatty acids and trans-fatty acids), to guide effective public health nutrition policies and programmes to promote a healthy diet.

There are some studies showing the inverse correlation between sugar intake and body weight, i.e. those with higher sugars intake are less likely to be overweight.

A systematic review was conducted to review the available evidence related to the intake of free sugars and weight gain, and recommendations were made based primarily on the evidence from the meta-analysis of randomized controlled trials comparing higher versus lower sugars intakes on body weight. Overall, the cohort studies included in the systematic review did not contradict the findings of the meta-analysis.

An ILSI-supported re-analysis of the IOM “Appendix J: Association of Added Sugars Intake and Intake of Other Nutrients” (2002) showed that those in the analysis with low added sugars intake (< 5 percent of energy) had a similar BMI to those with high added sugars intake (> 35 percent of energy): 28.9 compared to 28.1, respectively. Of persons who were overweight or obese, the highest proportions reported consuming between 5 and 15 percent of their energy from added sugars. With each 5 percent increase in added sugars intake above 15 percent added sugars intake, a lower prevalence of overweight and obese individuals was found, until the highest category of sugars intake was reached (>35 percent).

Inclusion and exclusion criteria used in selecting studies were guided by the PICO questions which are described in detail in Annex 6 of the guideline, and in the systematic review by Te Morenga et al. (2013). Results of the ILSI-supported analysis are noted, however this analysis was not included in the systematic review of evidence for free sugars intake and weight gain as it was not identified as meeting the inclusion criteria for the systematic review.

In 2013, Cancer Council Western Australia undertook a review of the literature on the effect of sugar-sweetened beverages consumption on health. The conclusions drawn were consistent with the WHO draft guidelines on sugars; there was a positive association between consumption of added sugars and body weight.

Comment noted.

Regarding free sugar intake and obesity the currently accepted causal pathway is: Excess energy intake -> positive energy balance -> obesity -> noncommunicable disease. An alternative causal pathway would be: Factor X (excess free sugar intake?) impacting both obesity and NCDs

Comment noted.

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directly in addition to a possible interaction of obesity and NCDs. There is mounting evidence of the latter hypothesis – as is evidenced by the phenomena of metabolically obese lean individuals and metabolically lean obese individuals. Recent evidence suggests that dietary sugars may be independently associated with higher blood pressure, coronary heart disease and cardiovascular mortality and that reducing consumption of sugar-sweetened beverages and dietary sugars are associated with reduced blood pressure.

A recent systematic review by Te Morenga et al. (2014) and large observational study by Yang et al. (2014) provide evidence supporting an association with cardiovascular disease risk factors.

The most recent studies show no correlation between mortality and sugars intake across a wide range of sugars intake.

A recent observational study by Yang et al. (2014) identified a significant relationship between added sugar consumption and increased risk for cardiovascular disease mortality, noting that those consuming less than 10% of calories as added sugars had lower risk than those consuming more.

Frequency of sugars consumption, and not amount, is the most important risk factor for dental caries. Other factors that may affect risk of dental caries include stickiness or viscosity of foods, presence of compounds that can inhibit the activity of oral pathogens, microflora in the mouth, acidity of foods and beverages, the potential of consumed food to stimulate saliva production, whether or not one smokes, fluoride exposure, oral hygiene and socioeconomic status. These are not considered in the guideline.

With respect to amount vs. frequency of sugars intake and risk of dental caries, the evidence review shows that both are important. But few studies have measured both variables simultaneously to enable the relative importance of these variables to be judged while there is a greater wealth of evidence pertaining to amount of sugars and dental caries. The studies that have measured both frequency and amount of sugars simultaneously in the same population (e.g. RuggGunn et al. [1984], Rodrigues et al. [1999]) have found that the two variables are correlated. Reducing the frequency of free sugars intake in the absence of a reduction of amount will not reduce the risk of not only dental caries, but also unhealthy weight gain and NCDs as a whole. Regarding the effects of viscosity of food and consumption of starches, the evidence review was also conducted by the 2002 WHO/FAO Expert Consultation and data did not suggest their more decisive role than the amounts of sugars consumed. As far as oral hygiene is concerned, it is indicated in a number of studies that when oral hygiene is controlled for, the relationship between sugars intake and dental caries still exists. Various references included in both the systematic review and the guideline provided data on these issues including Rugg-Gunn et al. (1984), Ruottinen et al. (2004), Rodrigues et al. (1999), WHO (2003). 25

Other factors (as listed in the above comment) affecting risk of dental caries were not considered in the systematic review and may have confounded the results obtained from the studies included in the review.

There is not strong evidence that these factors have a significant role to play in caries risk, independent of free sugars. The relationship between sugars intake and dental caries persists in the presence of exposure to fluoride, for instance. The cohort studies in the GRADE analysis all considered exposure to fluoride which did not differ between both lower and higher sugars groups. The GRADE analysis took into account the fact that ecological studies did not consider confounding factors and the quality of the evidence was downgraded accordingly.

Possible confounders of studies of sugars intake and dental caries, include adequate dental care and exposure to fluorides (e.g. drinking water, toothpaste, etc.). However, even with good dental care there is a progressive increase in the incidence of dental caries if sugar intakes are high. Also, fluoride can reduce, but does not entirely prevent the development of dental caries.

Comment noted.

Reducing free sugars intake is presented as a means to reduce the risk of dental caries. However, water fluoridation, access to dental care and good oral hygiene (including the use of fluoride toothpaste) are all very effective at reducing the risk of dental caries and have been responsible for significant reductions in dental caries in many populations worldwide. These are not adequately discussed in the guideline.

The guideline acknowledges that such practices have reduced the prevalence of dental diseases significantly. However, it also notes that a number of studies show that when oral hygiene is controlled for, the relationship between sugars intake and dental caries still exists.

The evidence presented does not take into consideration oral hygiene. It is unlikely that consumption of free sugars will increase risk of dental caries if proper oral hygiene is practiced. It would be better to state that the benefits (in terms of reducing risk of dental caries) associated with reducing free sugars intake to below 5% of total energy intake doesn't apply to populations with proper oral hygiene.

Noted in guideline that dental caries persists even when populations are exposed to fluoride (e.g. from oral hygiene).

Many mid- and high-income countries with higher intakes of free sugars (i.e. greater than 10% of total energy) now have lower caries prevalence than many of the countries with low sugars intake as a result of water fluoridation, improved dental care and improved oral hygiene.

The guideline acknowledges that such practices have reduced the prevalence of dental diseases significantly, in children. However, it is also noted that dental caries persists even in fluoridated populations and progresses with age.

Even in some high-income countries, water fluoridation is not universal and barriers to

Comment noted.

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obtaining adequate oral health care exist. Countries with estimated intake of sugars below 10% or 5% of total energy intake do not invariably have low caries prevalence.

Five population studies in the systematic review that allowed comparison of dental caries when sugars intake was below 10% of total energy intake compared with above 10% of total energy intake, showed lower caries when sugars intake was below 10% of total energy intake. There are few data from countries with intakes below 5% of total energy intake.

Evidence that dietary sugars are the major cause of dental caries comes from a wide spectrum of sources including human intervention studies, human observational studies, extensive animal studies, in vivo short-term studies, laboratory studies.

Comment noted.

There is a substantial body of scientific evidence indicating that free sugars are not uniquely responsible for dental caries. All fermentable carbohydrates (including some starches) can cause dental caries.

There is convincing evidence that non-processed starches are not associated with dental caries. Plaque pH and enamel slab experiments suggest that processed starches are acidogenic, but these data are not backed up with epidemiological studies. There are very few longitudinal data on the impact of processed starches on caries increment and only one paper has shown a non-significant trend (p8 weeks) controlled trials of the effect of increased or decreased free sugars intake on body weight not limited to children, but in free-living individuals, as well as the need to assess thresholds related to the risk of unhealthy weight gain, are noted in the “Implications for future research” section of the guideline.

The implications of eliminating fruit juices and fruit juice concentrates in the food supply on dietary intake of essential vitamins and minerals should be investigated.

The guideline is not recommending the elimination of fruit juices and fruit juice concentrates in the food supply. The recommendations are to reduce the levels of free sugars intake, of which fruit juices and fruit juice concentrates are a part.

Research is needed to investigate the consequences of labelling fruit juices and fruit juice concentrates as sources of ”free sugars” on consumers’ food choices and their nutritional status.

Comment noted.

Further research is needed to identify what works best to reduce obesity in large community settings and the way in which governments can best invest in different research.

Comment noted.

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